Compounds > 4-(5-(4-bromophenyl)-3-(6-methyl-2-oxo-4-phenyl-1-2-dihydroquinolin-3-yl)-4-5-dihydro-1h-pyrazol-1-yl)-4-oxobutanoic-acid

4-(5-(4-bromophenyl)-3-(6-methyl-2-oxo-4-phenyl-1-2-dihydroquinolin-3-yl)-4-5-dihydro-1h-pyrazol-1-yl)-4-oxobutanoic-acid and Tuberous-Sclerosis

4-(5-(4-bromophenyl)-3-(6-methyl-2-oxo-4-phenyl-1-2-dihydroquinolin-3-yl)-4-5-dihydro-1h-pyrazol-1-yl)-4-oxobutanoic-acid has been researched along with Tuberous-Sclerosis* in 1 studies

Other Studies

1 other study(ies) available for 4-(5-(4-bromophenyl)-3-(6-methyl-2-oxo-4-phenyl-1-2-dihydroquinolin-3-yl)-4-5-dihydro-1h-pyrazol-1-yl)-4-oxobutanoic-acid and Tuberous-Sclerosis

ArticleYear
Selective suppression of excessive GluN2C expression rescues early epilepsy in a tuberous sclerosis murine model.
    Nature communications, 2014, Aug-01, Volume: 5

    Tuberous sclerosis complex (TSC), caused by dominant mutations in either TSC1 or TSC2 tumour suppressor genes is characterized by the presence of brain malformations, the cortical tubers that are thought to contribute to the generation of pharmacoresistant epilepsy. Here we report that tuberless heterozygote Tsc1(+/-) mice show functional upregulation of cortical GluN2C-containing N-methyl-D-aspartate receptors (NMDARs) in an mTOR-dependent manner and exhibit recurrent, unprovoked seizures during early postnatal life (

    Topics: Action Potentials; Animals; Anticonvulsants; Disease Models, Animal; Electroencephalography; Epilepsy; Gene Expression Regulation; Heterozygote; Humans; Male; Mice; Mice, Transgenic; Microtomy; Neocortex; Patch-Clamp Techniques; Pyrazoles; Quinolones; Receptors, N-Methyl-D-Aspartate; Signal Transduction; Tissue Culture Techniques; TOR Serine-Threonine Kinases; Tuberous Sclerosis; Tuberous Sclerosis Complex 1 Protein; Tumor Suppressor Proteins

2014